Neuromuscular electrical stimulation is well known in the art and is used for a variety of clinical applications, including as a method for strengthening skeletal muscles. Typically, a conventional protocol of preset frequency, duration and intensity of electrical stimulation is prescribed to a patient (Stackhouse 2008). Electrical stimulation, particularly electromyogram (EMG)-triggered neuromuscular stimulation, has been used for many years in clinical settings to facilitate post-stroke motor recovery of finger extension impairments (Heckmann et al. 1997; Chae et al. 1998; Francisco et al. 1998; Cauraugh et al. 2000; Crisan and Garner 2001; Cauraugh and Kim 2002; Bocker and Smolenski 2003; Chae 2003; Bolton et al. 2004; de Kroon et al. 2005).
Roughly one third of all patients who experience a stroke have some residual impairment of the upper extremity (Parker et al. 1986; Gray et al. 1990; Nakayama et al. 1994), with a major impairment being of hand function (Trombly 1989). Common post-stroke hand function impairments include a stereotypically flexed resting posture of the wrist and fingers and an inability to extend fingers voluntarily. According to the literature, the contributing factors include biomechanical alterations, such as muscle atrophy (O'Dwyer et al. 1996); contractures (Metoki et al. 2003) and increased muscle stiffness (Dietz et al. 1991; Ibrahim et al. 1993); and neurological changes, such as wrist and finger flexor hypertonia—spasticity (Powers et al. 1988; Powers et al. 1989; Thilmann et al. 1991; Kamper and Rymer 2000; Kamper and Rymer 2001; Kamper et al. 2003), excessive coactivation of flexors and extensors (Hammond et al. 1988; Dewald et al. 1995), and reduced reciprocal inhibition (Nakashima et al. 1989; Baykousheva-Mateva and Mandaliev 1994). A recent study assessed the relative contributions of these mechanisms to overall finger and hand impairment in chronic hemiparetic stroke survivors and found that weakness in grip strength and finger extension strength accounted for the greatest portion of deficits in hand motor control after stroke (Kamper et al. 2006). As such, strengthening of finger (wrist) extensors and spasticity reduction in finger flexors are extremely important for improvement of hand function in stroke patients.
The EMG-triggered electrical stimulation protocol involves initiation by the patient of a voluntary contraction for a specific movement until the muscle activity (as measured by EMG) reaches a threshold level. When the muscle activity reaches the threshold level, it triggers an electrical stimulus to the target muscles, which facilitates the patient's movements (Heckmann et al. 1997; Chae et al. 1998; Francisco et al. 1998; Cauraugh et al. 2000; Crisan and Garner 2001; Cauraugh and Kim 2002; Bocker and Smolenski 2003; Chae 2003; Bolton et al. 2004; de Kroon et al. 2005). This intervention protocol has been found superior to passive neuromuscular stimulation in motor recovery, most likely due to the active engagement of patients during electrical stimulation therapy (Chae and Yu 2000; Chae 2003; Bolton et al. 2004; Kimberley et al. 2004). Electrical stimulation has been shown to produce immediate reductions in spasticity that may last from minutes to a few hours (Dewald et al. 1996). It has been reported that long-term users (greater than 16 months) may have longer lasting reductions in spasticity (Apkarian and Naumann 1991). However, the effectiveness of current electrical stimulation techniques on spasticity reduction remains controversial (Stackhouse 2008).
Further, the use of EMG-triggered electrical stimulation is associated with a few disadvantages, including in the finger/wrist rehabilitation context. First, EMG-triggered electrical stimulation requires voluntary activation of the muscles, by finger/wrist extension, to a certain preset threshold level. This requirement limits its application, especially for patients with moderately to severely impaired finger extension. Second, it requires “clean” EMG signals from the targeted muscle(s). This may be problematic when surface EMG signals are utilized. Though improved by using intramuscular EMG signals, this technique imposes other problems, including convenience, compliance and cost. Lastly and most importantly, inappropriate coactivation of finger flexors and extensors may cause serious problems when using assisted electrical stimulation (Kamper and Rymer 2001). For example, when patients try to assist the stimulation to the finger extensors, hand opening is significantly reduced due to inappropriate coactivation (Kamper and Rymer 2001) and finger flexor hypertonia (Chae and Hart 2003). Kamper and Rymer observed that attempts of voluntary metacarpao-phalangeal (MCP) joint extension actually resulted in MCP joint flexion in some hemiparetic patients (Kamper and Rymer 2001).
The clinical applications of EMG-triggered electrical stimulation for wrist/finger motor recovery are thus limited, and similar drawbacks to those discussed above are associated with EMG-triggered electrical stimulation in the other applications for which it is available. Moreover, as noted, passive neuromuscular stimulation has been found inferior to EMG-triggered stimulation for motor recovery.
Therefore, it would be desirable to have an improved system for delivering electrical stimulation to skeletal muscles.